Patients with subarachnoid hemorrhage (SAH) often exhibit cardiac abnormalities. Preliminary data from our current studies indicate that these abnormalities may be due to increases in sympathetic nervous system (SNS) activity and circulating levels of inflammatory cytokines (ICs). Our general hypothesis is that activation of the SNS and increases in ICs lead to cardiac dysfunction, reduced blood pressure, and cardiac output, ultimately increasing the risk of poor neurologic outcome after SAH. The Specific Aims of this proposal are as follows: 1. To test the hypothesis that specific single nucleotide polymorphisms (SNPs) of the beta- and alpha-adrenergic receptors are associated with an increased risk of developing cardiac injury (release of cardiac troponin I) and dysfunction (reduced left ventricular ejection fraction) after SAH. 2. To test the hypothesis that elevated plasma levels of norepinephrine and epinephrine are associated with an increased risk of developing cardiac injury and dysfunction after SAH. 3. To test the hypothesis that specific SNPs of the genes encoding ICs are associated with an increased risk of developing cardiac injury and dysfunction after SAH. 4. To test the hypothesis that elevated levels of ICs, including tumor necrosis factor-alpha, interleukin-1, and interleukin-6, are associated with an increased risk of developing cardiac injury and dysfunction after SAH. 5. To test the hypothesis that SAH-induced cardiac dysfunction is associated with decreased systolic blood pressure and increased inpatient mortality.